ライフサイエンスコーパス: fatty acid amide

1 tertiary amines) and endogenous metabolites (fatty acid amides).

2 tion to FAAH that could hydrolyze long-chain fatty acid amides.

3 molecules collectively known as the primary fatty acid amides.

4 class of endogenous signaling lipids termed fatty acid amides.

5 tified in Stevia for the first time, such as fatty acid amides.

6 the main enzyme catabolizing endocannabinoid fatty acid amides.

7 amily of bioactive signalling molecules, the fatty-acid amides.

8 lead to additional insights into the role of fatty acid amide activity in human biological systems an

9 ounds such as sebacates, adipates, citrates, fatty acid amides, among others.

10 5 eCBs and related compounds, including both fatty acid amides and glycerols.

11 hatic hydrocarbon resin), including alkanes, fatty acids, amides, and tackifying terpenoids embedded

12 Primary fatty acid amides are a group of bioactive lipids that h

13 discovered and solved the structures of six fatty acid amides as the products of the CD-enriched BGC

14 osynthesis, and its proposed role in primary fatty acid amide biosynthesis has been controversial.

15 at these proteins may collaborate to control fatty acid amide catabolism in primates.

16 n lowering plasma total cholesterol than the fatty acid amide CI-976.

17 The most prevalent elicitors are fatty acid amides consisting of 18-carbon polyunsaturate

18 Fatty acid amides constitute a large and diverse class o

19 Therefore, formulating the long-chain fatty acid amide derivatives of nucleoside analogs into

20 ng the active clades included a biohopanoid, fatty acid amides, diketopiperazines, lipid derivatives,

21 nnabinoid and endocannabinoid-like bioactive fatty acid amides during hibernation.

22 No appreciable amounts of fatty acid amides (e.g., oleamide), ceramides, or monoac

23 her elicitors including volicitin, the first fatty acid amide elicitor identified in caterpillars.

24 ATP-independent in vitro biosynthesis of the fatty acid amide elicitor, N-linolenoyl-l-glutamine, by

25 , a highly selective and orally bioavailable fatty acid amide (FAA) hydrolase inhibitor, was evaluate

26 he enzyme responsible for the degradation of fatty acid amides (FAA) including anandamide (AEA), palm

27 Fatty acid amides (FAAs) constitute a large class of end

28 y endogenous signalling compounds, including fatty acid amides (FAAs), chemical mimics of which are m

29 finding of oleamide and other members of the fatty acid amide family in the tear film could lead to a

30 n integral membrane enzyme that degrades the fatty acid amide family of endogenous signaling lipids,

31 n integral membrane enzyme that degrades the fatty acid amide family of signaling lipids, including t

32 is the best-understood member of the primary fatty acid amide family.

33 Fatty acid amide hydrolase (EC 3.5.1.4.) is the enzyme r

34 Here we show that mice lacking the enzyme fatty acid amide hydrolase (FAAH(-/-)) are severely impa

35 ates a common human mutation in the gene for fatty acid amide hydrolase (FAAH) (C385A; rs324420), the

36 aint stress, which results in an increase in fatty acid amide hydrolase (FAAH) activity and a reducti

37 Fatty acid amide hydrolase (FAAH) activity in mammals ha

38 A decrease in fatty acid amide hydrolase (FAAH) activity increases the

39 el fluorescent assay to continuously monitor fatty acid amide hydrolase (FAAH) activity that is simpl

40 cells, and then anandamide is hydrolyzed by fatty acid amide hydrolase (FAAH) and 2-AG by monoacylgl

41 paradigm to exert combined activity at human fatty acid amide hydrolase (FAAH) and dopamine receptor

42 rotein that may modulate CB(1) function; and fatty acid amide hydrolase (FAAH) and N-acylethanolamine

43 e and lower activity of its catabolic enzyme fatty acid amide hydrolase (FAAH) are associated with sc

44 hibitors 3-5 bound to a humanized variant of fatty acid amide hydrolase (FAAH) are disclosed and comp

45 Monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH) are two enzymes from t

46 h, we report the molecular identification of fatty acid amide hydrolase (FAAH) as a second intracellu

47 c enzymes, monoacylglycerol lipase (MAGL) or fatty acid amide hydrolase (FAAH) attenuates naloxone-pr

48 Fatty acid amide hydrolase (FAAH) controls brain anandam

49 Inhibition of the enzyme fatty acid amide hydrolase (FAAH) counteracts reward-rel

50 Fatty acid amide hydrolase (FAAH) degrades 2 major class

51 Fatty acid amide hydrolase (FAAH) degrades NAE into etha

52 Fatty acid amide hydrolase (FAAH) degrades neuromodulati

53 Fatty acid amide hydrolase (FAAH) degrades the endocanna

54 Fatty acid amide hydrolase (FAAH) degrades the endocanna

55 Measuring uptake at 25 s, when fatty acid amide hydrolase (FAAH) does not appreciably a

56 dized by lipoxygenase (LOX) or hydrolyzed by fatty acid amide hydrolase (FAAH) during normal seedling

57 Remarkably, fatty acid amide hydrolase (FAAH) expression, responsibl

58 ocannabinoid anandamide due to inhibition of fatty acid amide hydrolase (FAAH) facilitates fear extin

59 Here, we characterize a fatty acid amide hydrolase (FAAH) from a growth-associat

60 structures of the signal-terminating enzyme fatty acid amide hydrolase (FAAH) from Arabidopsis in it

61 In this report, we isolated the enzyme fatty acid amide hydrolase (FAAH) from mouse serum as an

62 he action of diverse hydrolases, among which fatty acid amide hydrolase (FAAH) has been well characte

63 The integral membrane enzyme fatty acid amide hydrolase (FAAH) hydrolyzes the endocan

64 Fatty acid amide hydrolase (FAAH) hydrolyzes the endocan

65 tigated the role of the AEA-degrading enzyme fatty acid amide hydrolase (FAAH) in AEA-induced cell de

66 holipase D (NAPE-PLD) and its degradation by fatty acid amide hydrolase (FAAH) in mouse embryos and o

67 holipase D (NAPE-PLD) and its degradation by fatty acid amide hydrolase (FAAH) in mouse embryos and o

68 g through inhibition of its catabolic enzyme fatty acid amide hydrolase (FAAH) in the basolateral com

69 ain lipids regulated by the mammalian enzyme fatty acid amide hydrolase (FAAH) in vivo, including kno

70 lly mediated by the integral membrane enzyme fatty acid amide hydrolase (FAAH) in vivo.

71 Fatty acid amide hydrolase (FAAH) inactivates a large an

72 Fatty acid amide hydrolase (FAAH) inactivates the endoge

73 CB(1)R signalling, as well as fatty acid amide hydrolase (FAAH) inhibition, are associ

74 A recent phase 1 trial of the fatty acid amide hydrolase (FAAH) inhibitor BIA 10-2474

75 We found that both the fatty acid amide hydrolase (FAAH) inhibitor URB597 and t

76 l finding that posttraining infusions of the fatty acid amide hydrolase (FAAH) inhibitor URB597, whic

77 The peripherally restricted fatty acid amide hydrolase (FAAH) inhibitor URB937 (3, c

78 ntified benzothiazole analogue 3 as a potent fatty acid amide hydrolase (FAAH) inhibitor.

79 nd characterization of alpha-ketoheterocycle fatty acid amide hydrolase (FAAH) inhibitors are disclos

80 nd urea derivatives are important classes of fatty acid amide hydrolase (FAAH) inhibitors that carbam

81 Fatty acid amide hydrolase (FAAH) is a degradative enzym

82 The metabolism of these lipids by fatty acid amide hydrolase (FAAH) is a key regulatory po

83 Fatty acid amide hydrolase (FAAH) is a mammalian amidase

84 Fatty acid amide hydrolase (FAAH) is a mammalian integra

85 Fatty acid amide hydrolase (FAAH) is a mammalian integra

86 Fatty acid amide hydrolase (FAAH) is a mammalian integra

87 Fatty acid amide hydrolase (FAAH) is a membrane-bound en

88 Fatty acid amide hydrolase (FAAH) is a membrane-bound en

89 Fatty acid amide hydrolase (FAAH) is a pharmaceutical ta

90 Fatty acid amide hydrolase (FAAH) is a serine hydrolase

91 Fatty acid amide hydrolase (FAAH) is a serine hydrolase

92 Fatty acid amide hydrolase (FAAH) is an enzyme responsib

93 Fatty acid amide hydrolase (FAAH) is an integral membran

94 Fatty acid amide hydrolase (FAAH) is an integral membran

95 Fatty acid amide hydrolase (FAAH) is an integral membran

96 evels of endocannabinoids with inhibitors of fatty acid amide hydrolase (FAAH) is analgesic in models

97 Fatty acid amide hydrolase (FAAH) is one of the main enz

98 Once transported into the cytoplasm, fatty acid amide hydrolase (FAAH) is responsible for met

99 Fatty acid amide hydrolase (FAAH) knockout mice are pron

100 y-state time points (5 min), suggesting that fatty acid amide hydrolase (FAAH) may be responsible for

101 liana, and they can be metabolized by either fatty acid amide hydrolase (FAAH) or by lipoxygenase (LO

102 cal inhibition or genetic deletion of either fatty acid amide hydrolase (FAAH) or monoacylglycerol li

103 Fatty acid amide hydrolase (FAAH) plays a key role in re

104 In mice, pharmacological inhibition of fatty acid amide hydrolase (FAAH) produces elevated leve

105 Since stress-induced activation of fatty acid amide hydrolase (FAAH) reduces AEA, we confir

106 ngle nucleotide polymorphisms CNR1 rs806378, fatty acid amide hydrolase (FAAH) rs324420, and MGLL rs4

107 Fatty acid amide hydrolase (FAAH) terminates the endocan

108 were prepared and examined as inhibitors of fatty acid amide hydrolase (FAAH) that additionally targ

109 of an inhibitor of the AEA catabolic enzyme fatty acid amide hydrolase (FAAH) to afford pain relief

110 A binding assay for human fatty acid amide hydrolase (FAAH) using the scintillatio

111 eral principle, the serine hydrolytic enzyme fatty acid amide hydrolase (FAAH) was found to degrade a

112 We show here that mice devoid of fatty acid amide hydrolase (FAAH) with elevated levels o

113 rease in side population (SP) cells, whereas fatty acid amide hydrolase (FAAH)(-/-) mice, which have

114 Fatty acid amide hydrolase (FAAH), a gene in the minimal

115 azole inhibitors (1 (OL-135) and 2) bound to fatty acid amide hydrolase (FAAH), a key enzymatic regul

116 ce of the eCB N-arachidonoylethanolamine via fatty acid amide hydrolase (FAAH), although it is unclea

117 Fatty acid amide hydrolase (FAAH), an amidase-signature

118 AEA is hydrolyzed by fatty acid amide hydrolase (FAAH), an enzyme localized o

119 l structure of the integral membrane protein fatty acid amide hydrolase (FAAH), an enzyme that degrad

120 prodrug strategy targets a specific amidase, fatty acid amide hydrolase (FAAH), an enzyme with enrich

121 endocytosis, and finally, to be degraded by fatty acid amide hydrolase (FAAH), an integral membrane

122 ting that following metabolism by the enzyme fatty acid amide hydrolase (FAAH), anandamide metabolite

123 endocannabinoid anandamide is hydrolysis by fatty acid amide hydrolase (FAAH), and inhibitors of the

124 erminated following hydrolysis by 2 enzymes: fatty acid amide hydrolase (FAAH), and the less-studied

125 L activity as well as their selectivity over fatty acid amide hydrolase (FAAH), another endocannabino

126 mes have been considered to serve this role: fatty acid amide hydrolase (FAAH), cyclooxygenase-2 (COX

127 The intracellular serine amidase, fatty acid amide hydrolase (FAAH), degrades a heterogene

128 e, such as monoacylglycerol lipase (MGL) and fatty acid amide hydrolase (FAAH), in a selective manner

129 ype 2 diabetes, and VHH nanobodies targeting Fatty Acid Amide Hydrolase (FAAH), involved in chronic p

130 nships of 2b (OL-135), a potent inhibitor of fatty acid amide hydrolase (FAAH), is detailed targeting

131 (SAR) of 2f (OL-135), a potent inhibitor of fatty acid amide hydrolase (FAAH), is detailed, targetin

132 ated by several metabolic enzymes, including fatty acid amide hydrolase (FAAH), monoacylglycerol lipa

133 inhibition of cyclooxygenase-2 (COX-2), not fatty acid amide hydrolase (FAAH), prolongs DSI, suggest

134 hibition of the anandamide-degrading enzyme, fatty acid amide hydrolase (FAAH), prolongs the regulato

135 hrough inhibition of its degradative enzyme, fatty acid amide hydrolase (FAAH), restored both synapti

136 on, cloning, and expression of a rat enzyme, fatty acid amide hydrolase (FAAH), that degrades bioacti

137 incipal endocannabinoid-inactivating enzyme, fatty acid amide hydrolase (FAAH), that in homozygous fo

138 Reductions in fatty acid amide hydrolase (FAAH), the catabolic enzyme

139 eripherally restricted inhibitor (URB937) of fatty acid amide hydrolase (FAAH), the enzyme responsibl

140 JNJ-42165279 is a selective inhibitor of fatty acid amide hydrolase (FAAH), the enzyme responsibl

141 TFNO, an inhibitor of fatty acid amide hydrolase (FAAH), the enzyme responsibl

142 opment of exceptionally potent inhibitors of fatty acid amide hydrolase (FAAH), the enzyme responsibl

143 ate endocannabinoid signalling by inhibiting fatty acid amide hydrolase (FAAH), the enzyme that degra

144 We also found that fatty acid amide hydrolase (FAAH), the enzyme that metab

145 issense variant Pro129Thr of the gene coding fatty acid amide hydrolase (FAAH), the major degrading e

146 Inhibition of fatty acid amide hydrolase (FAAH), the primary enzyme fo

147 cluding the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH), triacylglycerol hydro

148 inhibition of endocannabinoid transport and fatty acid amide hydrolase (FAAH), two mechanisms of end

149 ignaling related to a common polymorphism in fatty acid amide hydrolase (FAAH), which alters endocann

150 HR1), evokes a rapid induction of the enzyme fatty acid amide hydrolase (FAAH), which causes a reduct

151 t (rs324420) in the gene encoding the enzyme fatty acid amide hydrolase (FAAH), which degrades NAEs,

152 that promotes the cellular uptake of AEA and fatty acid amide hydrolase (FAAH), which hydrolyzes AEA

153 g activity is terminated by an enzyme called fatty acid amide hydrolase (FAAH), which hydrolyzes NAEs

154 bition of endocannabinoid hydrolyzing enzyme fatty acid amide hydrolase (FAAH), which leads to increa

155 hypoxic pulmonary vasoconstriction (HPV) via fatty acid amide hydrolase (FAAH)-dependent metabolites.

156 d 2-arachidonylglycerol) degradative enzyme, fatty acid amide hydrolase (FAAH)-IR, in the rat retina.

157 t negative growth-regulating properties, and fatty acid amide hydrolase (FAAH)-mediated hydrolysis is

158 iological processes, which are terminated by fatty acid amide hydrolase (FAAH).

159 tors of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH).

160 AEs) are primarily inactivated by the enzyme fatty acid amide hydrolase (FAAH).

161 unction with increased degradation of AEA by fatty acid amide hydrolase (FAAH).

162 were prepared and examined as inhibitors of fatty acid amide hydrolase (FAAH).

163 gulated by monoacylglycerol lipase (MGL) and fatty acid amide hydrolase (FAAH).

164 potent and systemically active inhibitor of fatty acid amide hydrolase (FAAH).

165 ovalent inhibitor of the EC-degrading enzyme fatty acid amide hydrolase (FAAH).

166 cted only in cells overexpressing the enzyme fatty acid amide hydrolase (FAAH).

167 es pertaining to mechanical nociception, and fatty acid amide hydrolase (FAAH).

168 ediate AEA transport to its catabolic enzyme fatty acid amide hydrolase (FAAH).

169 strates for firefly luciferase by the enzyme fatty acid amide hydrolase (FAAH).

170 reduced activity of the AEA-degrading enzyme fatty acid amide hydrolase (FAAH).

171 es higher levels of the anandamide hydrolase fatty acid amide hydrolase (FAAH).

172 andamide is degraded by the catabolic enzyme fatty acid amide hydrolase (FAAH).

173 ing the anandamide-degrading membrane enzyme fatty acid amide hydrolase (FAAH).

174 s a potent in vitro and in vivo inhibitor of fatty acid amide hydrolase (FAAH).

175 nhibits cyclooxygenase-1 (COX-1), COX-2, and fatty acid amide hydrolase (FAAH).

176 bitors of monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH).

177 n between genetically inherited variation in fatty acid amide hydrolase (FAAH, C385A), which metaboli

178 Fatty acid amide hydrolase (FAAH, EC 3.5.1.99) is the ma

179 Mice lacking the enzyme fatty acid amide hydrolase [FAAH (-/-) mice] are severel

180 Nicotine exposure had no effect on fatty acid amide hydrolase activity in the VTA, suggesti

181 pharmacological profile in that it inhibits fatty acid amide hydrolase and alpha/beta-hydrolase doma

182 ing protein 12, monoacylglycerol lipase, and fatty acid amide hydrolase and did not display affinity

183 duced synergistic antiallodynic effects with fatty acid amide hydrolase and monoacylglycerol lipase i

184 bitors of endocannabinoid-regulating enzymes fatty acid amide hydrolase and monoacylglycerol lipase p

185 verall, the MAH data are similar to those of fatty acid amide hydrolase and support the suggestion th

186 udies revealed that NAPE-phospholipase D and fatty acid amide hydrolase are expressed in intestinal e

187 nnabinol and anandamide potentiation through fatty acid amide hydrolase blockade.

188 nnabinol and anandamide potentiation through fatty acid amide hydrolase blockade.

189 s of NAGly and its degradation by the enzyme fatty acid amide hydrolase can be observed in rat brain

190 rgan radiation exposure for the irreversible fatty acid amide hydrolase enzyme probe (11)C-CURB is wi

191 FAAH, which encodes the anandamide-degrading fatty acid amide hydrolase enzyme.

192 modulation of emotional states and point to fatty acid amide hydrolase inhibition as an innovative a

193 ferences following the administration of the fatty acid amide hydrolase inhibitor AM374.

194 ibiting their metabolizing enzymes URB597 (a fatty acid amide hydrolase inhibitor) and JZL184 (a mono

195 Independently of E2, a fatty acid amide hydrolase inhibitor, which blocks break

196 is of a retinoic acid receptor agonist and a fatty acid amide hydrolase inhibitor.

197 e phytocannabinoid cannabidiol and selective fatty acid amide hydrolase inhibitors has been proposed,

198 PalGly was up-regulated in fatty acid amide hydrolase knockout mice, suggesting a p

199 , N-acyltaurines, was recently discovered in fatty acid amide hydrolase knockout mice.

200 By combining fatty acid amide hydrolase or monoacyl glycerol lipase i

201 AEs are hydrolyzed intracellularly by either fatty acid amide hydrolase or N-acylethanolamine-hydroly

202 cerol lipase paralogs (DAGLalpha, DAGLbeta), fatty acid amide hydrolase paralogs (FAAH1, FAAH2), mono

203 sion of the Arabidopsis NAE degrading enzyme fatty acid amide hydrolase resulted in seedlings that we

204 oxylipin metabolites were identified in FAAH fatty acid amide hydrolase seedlings but not in wild-typ

205 rts focused on pharmacological inhibition of fatty acid amide hydrolase to elevate levels of the endo

206 ve MAGL inhibitor JZL184, in Mgll(-/-) mice, fatty acid amide hydrolase(-/-) mice, and in cannabinoid

207 Preventing their degradation (by inhibiting fatty acid amide hydrolase) enhanced the effects of OEA

208 f uptake (resulting in signal termination by fatty acid amide hydrolase) has been elusive.

209 EA synthesis, without concomitant changes in fatty acid amide hydrolase, an enzyme responsible for OE

210 These data contrast with blockade of fatty acid amide hydrolase, an enzyme that degrades the

211 availability of the X-ray structures of Pam, fatty acid amide hydrolase, and malonamidase E2 has led

212 dentified at the molecular level (designated fatty acid amide hydrolase, FAAH), and although an analo

213 chemically and described as an inhibitor of fatty acid amide hydrolase, had previously been found in

214 As with another member of this family, fatty acid amide hydrolase, MAH has the uncommon ability

215 also show that dCAD cells express functional fatty acid amide hydrolase, the enzyme primarily respons

216 ective and systemically active inhibitors of fatty acid amide hydrolase, the enzyme responsible for t

217 th as oleamide agonists and as inhibitors of fatty acid amide hydrolase, which is responsible for the

218 he intracellular anandamide-degrading enzyme fatty acid amide hydrolase-1 (FAAH-1), termed FAAH-like

219 pathways can be suggested: 1) inhibition of fatty acid amide hydrolase-induced increases in anandami

220 ty and expression of the OEAdegrading enzyme fatty acid amide hydrolase.

221 1.80 fmol/mg protein) that is distinct from fatty acid amide hydrolase.

222 lism in cotton by inducing overexpression of fatty acid amide hydrolase.

223 entiation of the anandamide catabolic enzyme fatty acid amide hydrolase.

224 ivity of the anandamide-catabolizing enzyme, fatty acid amide hydrolase.

225 by monoacylglycerol lipase (MAGL) but not by fatty acid amide hydrolase.

226 e than N-arachidonoylserotonin in inhibiting fatty acid amide hydrolase.

227 y of the endocannabinoid metabolizing enzyme fatty acid amide hydrolase.

228 ing enzymes, the anandamide-degrading enzyme fatty acid amide hydrolase; or the 2-AG (2-arachidonoyl

229 ing enzymes, the anandamide-degrading enzyme fatty acid amide hydrolase; or the 2-AG (2-arachidonoyl

230 Fatty-acid amide hydrolase (FAAH) is a membrane-bound en

231 in those cells containing an amidase called fatty-acid amide hydrolase (FAAH) is hydrolysis to arach

232 internalization, anandamide is hydrolyzed by fatty-acid amide hydrolase (FAAH), an intracellular memb

233 regions with higher MAGL expression (but not fatty-acid amide hydrolase or FAAH) were more vulnerable

234 ill hereafter refer to oleamide hydrolase as fatty-acid amide hydrolase, in recognition of the plural

235 bitors of the anandamide-deactivating enzyme fatty-acid amide hydrolase, which selectively elevate an

236 transporter while being a poor substrate for fatty-acid amide hydrolase.

237 tion of arachidonic acid and ethanolamine by fatty-acid amide hydrolase.

238 The DEX effect was prevented by blocking fatty acid amide hydrolysis or by inhibiting anandamide

239 at oleamide hydrolase converts anandamide, a fatty-acid amide identified as the endogenous ligand for

240 ow the identification of fatty acids and the fatty acid amides in human meibomian gland secretions by

241 e, and human supports a general role for the fatty acid amides in mammalian biology.

242 anolamine-based compound and the presence of fatty acid amides in tissue prompts us to propose that p

243 Representative fatty acid amides include the N-acyl ethanolamines (NAEs

244 de hydrolase (FAAH) degrades neuromodulating fatty acid amides including anandamide (endogenous canna

245 nsible for the catabolism of neuromodulatory fatty acid amides, including anandamide and oleamide.

246 ng to the N-acyl ethanolamine (NAE) class of fatty acid amides, including the endocannabinoid anandam

247 ture enzyme that inactivates neuromodulatory fatty acid amides, including the endogenous cannabinoid

248 yme that catabolizes several neuromodulatory fatty acid amides, including the endogenous cannabinoid

249 he hydrolysis of a number of neuromodulatory fatty acid amides, including the endogenous cannabinoid

250 rolysis of a number of primary and secondary fatty acid amides, including the neuromodulatory compoun

251 Capsaicin, a vanillyl fatty acid amide (ingredient of hot pepper), released su

252 de hydrolase (FAAH), that degrades bioactive fatty acid amides like oleamide and anandamide to their

253 ne-bound enzyme that inactivates a family of fatty acid amide molecules which are implicated in physi

254 ified in a similar manner, as were the other fatty acid amides (myristamide, palmitamide, stearamide,

255 Fatty acid amides of polyamines may be rapidly cleared f

256 N4-Substituted fatty acid amide prodrugs of 10-16 carbon chain length d

257 vidence that PAM does have a role in primary fatty acid amide production in vivo.

258 ntly identified a second structural class of fatty acid amides regulated by FAAH in vivo: the N-acyl

259 The magnitude and duration of fatty acid amide signaling are controlled by enzymatic h

260 ntegrates into cell membranes and terminates fatty acid amide signaling in vivo.

261 elmidrol, an analog of the anti-inflammatory fatty acid amide signaling molecule palmitoylethanolamid

262 g genetic or pharmacological findings on the fatty acid amide signaling system across species.

263 sis, post-transcriptional gene silencing and fatty-acid amide signalling.

264 and membrane access channel responsible for fatty acid amide substrate and inhibitor acyl chain bind

265 ter as FAAH-1 and FAAH-2, hydrolyzed primary fatty acid amide substrates (e.g. oleamide) at equivalen

266 e-bound enzyme that degrades neuromodulatory fatty acid amides, such as oleamide and anandamide, and

267 phenolic acids, flavonoids, peptides, fatty acids/amides, sulfolipids, glucosinolates and caro

268 s) in M. sexta represents direct evidence of fatty acid amide synthesis by caterpillar tissues.

269 N-Acylethanolamines (NAEs) are a group of fatty acid amides that play signaling roles in diverse p

270 ydrolase, in recognition of the plurality of fatty-acid amides that the enzyme can accept as substrat

271 (FAAH) degrades 2 major classes of bioactive fatty acid amides, the N-acylethanolamines (NAEs) and N-

272 otransmitters, monoacylglycerols and primary fatty acid amides using 7 isotope labelled internal stan